Evidence for a role of calmodulin in serum stimulation of Na+ influx in human fibroblasts.
Sodium influx in serum-deprived human diploid fibroblasts can be stimulated by addition of serum (5-fold) or the divalent cation ionophore A23187 (3-fold). The possible involvement of calmodulin in serum or A23187 stimulation of Na+ influx has been investigated by using six psychoactive agents that are known to bind calmodulin and inhibit calmodulin-sensitive enzymes. Each agent inhibited serum- and A23187-stimulated Na+ influx in a dose-dependent manner. Furthermore, the K1 for inhibition of serum-stimulated Na+ influx correlates directly with the Ca2+-specific calmodulin binding previously determined in a cell-free system [Levin, R. M. & Weiss, B. (1979) J. Pharmacol. Exp, Ther. 208, 454--459]. None of the agents tested had any effect on the serum-insensitive component of net Na+ influx in these cells. These data support the concept that serum and A23187 stimulate Na+ influx in human diploid fibroblasts via an increase of intracellular Ca2+ and a subsequent calmodulin-mediated activation of the amiloride-sensitive transport pathway.
D001692:Biological Transport / Q000187:drug effects; D001769:Blood; D000001:Calcimycin / Q000037:antagonists & inhibitors; D002135:Calcium-Binding Proteins / Q000502:physiology*; D002147:Calmodulin / Q000037:antagonists & inhibitors / Q000502:physiology*; D002478:Cells, Cultured; D003470:Culture Media; D006801:Humans; D007700:Kinetics; D012964:Sodium / Q000378:metabolism*; D014268:Trifluoperazine / Q000494:pharmacology
D002135:Calcium-Binding Proteins; D002147:Calmodulin; D003470:Culture Media; D014268:Trifluoperazine; D000001:Calcimycin; D012964:Sodium